The present invention relates generally to implantable cardioverter defibrillators, and, more particularly, to a method for delivering cardiac therapy (e.g., defibrillation/shock therapy), and a cardiac therapy device (e.g., an ICD) for implementing the same.
Implantable cardioverter defibrillators (ICDs) are sophisticated medical devices which are surgically implanted (abdominally or pectorally) in a patient to monitor the cardiac activity of the patient's heart, and to deliver electrical stimulation as required to correct cardiac arrhythmias which occur due to disturbances in the normal pattern of electrical conduction within the heart muscle. Cardiac arrhythmias can generally be thought of as disturbances of the normal rhythm of the heart beat. Cardiac arrhythmias are broadly divided into two major categories, namely, bradyarrhythmia and tachyarrhythmia. Tachyarrhythmia can be broadly defined as an abnormally rapid heart rate (e.g., over 100 beats/minute, at rest), and bradyarrhythmia can be broadly defined as an abnormally slow heart rate (e.g., less than 50 beats/minute). Tachyarrhythmias are further subdivided into two major sub-categories, namely, tachycardia and fibrillation. Tachycardia is a condition in which the electrical activity and rhythms of the heart are rapid, but organized. Fibrillation is a condition in which the electrical activity and rhythm of the heart are rapid, chaotic, and disorganized. Tachycardia and fibrillation are further classified according to their location within the heart, namely, either atrial or ventricular. In general, atrial arrhythmias are not life-threatening, because the atria (upper chambers of the heart) are only responsible for aiding the movement of blood into the ventricles (lower chambers of the heart), whereas ventricular arrhythmias are life-threatening, because if the ventricles become arrhythmic, the heart's ability to pump blood to the rest of the body is impaired. The most serious and immediately life-threatening type of cardiac arrhythmia is ventricular fibrillation, in which the electrical activity of the ventricles becomes so random and chaotic that the heart rapidly becomes unable to pump sufficient blood to sustain life.
In general, an ICD continuously monitors the heart activity of the patient in whom the device is implanted by analyzing electrical signals, known as electrograms (EGMs), detected by endocardial (intracardiac) sensing electrodes positioned in the right ventricular apex and/or right atrium of the patient's heart. More particularly, contemporary ICDs include waveform digitization circuitry which digitizes the analog EGM produced by the sensing electrodes, and a microprocessor and associated peripheral ICs which analyze the digitized EGM in accordance with a diagnostic algorithm implemented by software stored in the microprocessor. Contemporary ICDs are generally capable of diagnosing the various types of cardiac arrhythmias discussed above, and then delivering the appropriate electrical stimulation/therapy to the patient's heart, in accordance with a therapy delivery algorithm also implemented in software stored in the microprocessor, to thereby correct or terminate the diagnosed arrhythmia.
In this connection, contemporary ICDs are capable of delivering various types or levels of electrical therapy. The first type of therapy is bradycardia and antitachycardia pacing, in which a low level of electrical energy (generally between millionths to thousandths of a joule) is delivered to the patient's heart in order to correct detected episodes of bradycardia or tachycardia, respectively. The second type of therapy is cardioversion, in which an intermediate level of electrical energy (generally between 1-5 joules) is delivered to the patient's heart in order to terminate a detected episode of ventricular tachycardia (e.g., a detected heart beat in the range of 130-190 beats/minute) or an ongoing episode of tachycardia that antitachycardia pacing has failed to correct or terminate. The third type of therapy is defibrillation, in which a high level of electrical energy (generally above 15 joules) is delivered to the patient's heart in order to abort a detected episode of ventricular fibrillation or an episode of ventricular tachycardia which has degraded into ventricular fibrillation due to failure of cardioversion therapy.
The provision of the above-described different types or levels of therapy is generally referred to in the art as "tiered therapy". In this regard, contemporary ICDs which are capable of delivering tiered therapy are sometimes referred to as combination pacemakers/defibrillators or as implantable cardioverter-defibrillators. As used herein, the terminology "implantable cardiac defibrillator" (ICD) is intended to encompass these and other forms and types of implantable cardiac therapy devices.
Current-generation ICDs which are capable of delivering tiered therapy provide several advantages over previous-generation ICDs which were only capable of delivering high energy defibrillation therapy. Namely, ICDs which are capable of delivering tiered therapy are generally more energy-efficient, since they can deliver much lower energy therapy, such as antitachycardia pacing and cardioversion, to terminate many arrhythmia events before they degrade into a ventricular fibrillation event. The much higher energy defibrillation therapy is only necessary when these lower energy therapies fail to abort the arrhythmia. Thus, tiered therapy conserves the energy stored in the battery(ies) of the device, thereby extending the longevity of the device, and also enables a significant portion of potential ventricular fibrillation events to be aborted with lower energy therapy which is much less painful and uncomfortable to the patient.
A primary goal in the design and further development of ICDs is to ensure delivery of effective therapy with a minimum expenditure of energy. Reduction of the total energy required to deliver effective therapy enables the size of the batteries and capacitors used in the ICDs to be reduced, thereby enabling a commensurate reduction in the size of the ICD. The benefits to the patient are two-fold. First, the use of lower voltage cardioversion and defibrillation therapy reduces patient pain and discomfort during delivery of such therapy, and second, the reduction in the size of the ICD decreases patient discomfort due to the physical pressure exerted by the ICD within the patient's body. A further benefit is that the longevity of the device can be extended for a given power supply. Additionally, the smaller the ICD, the easier it is to implant the device using minimally invasive surgery, thereby decreasing the cost of implantation. In this regard, it is highly preferable that the ICD be at least small enough to be implanted pectorally, rather than abdominally, without sacrificing functionality, because pectoral implantation requires much less invasive surgery than abdominal implantation. Consequently, pectoral implantation is both much less costly and much more comfortable to the patient (both at the time of implantation and thereafter), than abdominal implantation.
One of the major areas of ongoing R&D within the field of ICDs is the development of increasingly sophisticated diagnostic and therapy delivery algorithms, which enable the above-stated primary ICD design goal to be realized by optimizing the therapeutic efficacy of the device. More particularly, in accordance with the diagnostic algorithm, the microprocessor and associated peripheral ICs continuously monitor the digitized EGMs in order to sense or detect various features thereof, e.g., waveform slope (dv/dt), waveform minima and maxima, intervals between specified cardiac events, etc., which are indicative of various prescribed cardiac events, e.g., (P)QRS complexes, depolarization, repolarization, tachycardia, bradycardia, fibrillation, etc.
When a specified cardiac event is detected, the microprocessor, under the control of the therapy delivery algorithm, then triggers and controls the delivery of therapy, e.g., synchronous with (i.e., generally time-related to) such sensed features of the EGMs and/or cardiac events, in order to avoid inducing a degeneration to fibrillation in a tachycardia episode (i.e., arrhythmogenesis). In this regard, therapy is generally delivered (by the output or current delivery stage of the ICD, under microprocessor control) as a sequence of one or more electrical pulses, the timing, number, shape, tilt, magnitude, duration, and/or polarity (and/or other characteristics) of which are controlled in accordance with the therapy delivery algorithm in such a manner as to optimize therapeutic efficacy. The optimum values of the parameters or variables used in these algorithms may vary from one patient to the next, depending on the individual patient's particular cardiac condition and/or history.
Although the presently known therapy delivery algorithms have proven effective, it is believed that there is still room for improvement, and, more particularly, for a therapy delivery algorithm that ensures delivery of effective therapy with even lower energy requirements. In this connection, the present invention, in one of its aspects, is directed to a different approach to delivery of cardiac therapy in which the electrical activity in different regions of the heart is sensed and compared, and in which the timing of the electrical stimuli delivered to the heart is related to the results of the comparison. The present invention, in another of its aspects, is directed to a different approach to delivery of cardiac therapy in which activation intervals in different regions of the heart are selectively shortened or lengthened, based upon the sensed electrical activity in the different regions, to thereby reduce the energy required to terminate detected arrhythmias, e.g., to lower the defibrillation threshold (DFT) and thus, the overall energy required to deliver effective defibrillation therapy.
The following definitions and brief review of pertinent aspects of cardiology is designed to facilitate a better understanding of the ensuing description of the present invention. Starting first with the definitions, the term "electrogram" as used herein means "an extracellular unipolar or bipolar recording or a monophasic action potential (MAP)". The term "voltage gradient" as used herein means "the voltage across tissue that is created when a field stimulus is applied (measured in volts per centimeter)".
The term "action potential" as used herein means "a transient change in electric potential across the membrane of a myocardial cell in response to either an intrinsic or extrinsic electrical stimulus". The term "activation" as used herein means "the depolarization of tissue (phase 0 of action potential) locally to an electrogram". The term "refractory period" as used herein means "a period of time following an activation during which cardiac tissue repolarizes and will not produce a new activation in response to a further electrical stimulus (absolute refractory period), or will only produce a new activation in response to a further stimulus having a higher amplitude (relative refractory period). Further, the "refractory period" is a period during which an extension of the repolarization time of the tissue can occur, in response to an electrical stimulus which is not strong enough to produce a new activation, a phenomenon known as "refractory period extension".
The time period when a refractory period extension is induced is part of what has been previously clinically defined as an "absolute refractory period". As used herein, however, the term "refractory period" shall mean the entire period from the time that any refractory period extension can be induced by external stimuli until the time that the tissue has recovered complete excitability. The term "excitable gap" as used herein means "the period following an activation when tissue local to an electrogram recovers complete excitability". Thus, as used herein, "excitable gaps" correspond to the time periods (intervals) between successive activations, as can be seen in FIG. 1.
With ventricular tachycardia, a shortening of the normal cardiac cycle is experienced (i.e., the interval between successive heartbeats or "QRS complexes" decreases), thereby resulting in an elevated heart rate. Although the heart rate is elevated, the electrical activity of the myocardial cells distributed throughout the heart tissue is generally synchronous, i.e., the excitable gaps are generally synchronized, thereby stimulating the heart muscle to rhythmically contract and relax, to thereby produce successive heart beats, albeit at an elevated heart rate.
Atrial and ventricular fibrillation consist of multiple wavefronts traversing the heart at once. It has been shown that these wavefronts both converge and break up, creating periods of higher and lower organization. As will become apparent hereinafter, a goal of the therapy method of the present invention is to organize these wavefronts with a minimum amount of energy.
When a defibrillation shock is delivered by a shock delivery electrode, different voltage gradients are produced across different local regions of the heart, with the magnitude of the voltage gradients decreasing as a function of distance and position relative to the delivery electrodes, with the highest voltage gradient occurring right at the tissue/electrode interface. Thus, the voltage gradient (VG) across a region of the heart near the electrodes (hereinafter referred to as the "near-field region") will be significantly higher than the VG across a region of the heart which is more distant from the electrodes (hereinafter referred to as the "far-field region"). It is known that delivery of a pulse during the latter part of the refractory period of an action potential can prolong the duration of the action potential, and that the extent of the action potential prolongation is dependent upon the specific timing of the pulse (particularly with respect to the degree of membrane "repolarization") and the magnitude of the VG across the myocardial cells, so long as the magnitude of the pulse does not exceed a threshold level which, if exceeded, would create a new action potential.
It has been established that the above-described refractory period extension (RPE) or action potential prolongation is enhanced by delivering shocks having a biphasic waveform, as opposed to a monophasic waveform. See, e.g., the article entitled "Biphasic Defibrillation Waveforms Reduce Shock-Induced Response Duration Dispersion Between Low and High Shock Intensities", by Oscar H. Tovar, Janice L. Jones, Circ. Res. 1995; 77:430-438. In this regard, it is believed that the biphasic waveform reduces the disparity in shock-induced response durations between low and high voltage gradients as compared with the monophasic waveform. In other words, it is believed that the biphasic waveform produces a more uniform RPE of the action potentials in the different LVG regions of the heart. It has also been established that the RPE increases the later in the refractory period in which the shock is delivered. See, e.g., the article entitled "Ventricular Refractory Period Extension Caused by Defibrillation Shocks", by Robert J. Sweeney et al., Circulation 1990; 82:965-972.
It has also been shown that RPE is a very transient rescheduling of the cellular repolarization process, which is consistent with the hypothesis that RPE may result from a local graded response of the cells to the shock stimulus. It has further been shown that RPE is confined to the repolarization phase in which the shock is delivered, and that it is not caused by a transient change in cellular excitability.
The myocardial cells of different regions of the heart are in different phases of the action potential during fibrillation. In addition, a defibrillation shock creates differing VGs across different regions of the heart. Therefore, the shock can induce a wide variety of cellular responses simultaneously, either prolonging the refractory period so that the myocardial cells block re-entrant fibrillation wavefronts from propagating, or induce activations which can create new re-entry, or have no effect, such as when a shock is delivered in the early refractory period of cardiac tissue. Because of this, a shock can lead to refibrillation.
The "upper limit of vulnerability" hypothesis states that the shock must be strong enough to limit the "dispersion of refractoriness" below a critical threshold which leads to refibrillation. Of course, increasing the required strength of the shock (i.e., increasing the defibrillation threshold (DFT) and the defibrillation energy requirements) is just the opposite of the desired goal of defibrillation therapy. For successful defibrillation, it is believed that there must be a decrease in the dispersion of repolarization. As will become fully apparent hereinafter, the therapy delivery method of the present invention attempts to decrease the dispersion of repolarization by shortening and extending activation intervals in different regions of the heart, with the goal (in the presently preferred embodiment) of synchronizing the electrical activity throughout the entire heart.